Search results for "Neoplastic"

showing 10 items of 2901 documents

Antitumor effects of curcumin and structurally β-diketone modified analogs on multidrug resistant cancer cells

2007

Abstract Using concepts of bioisostery a series of curcumin analogs were synthesized: the diketonic system of the compound was elaborated into enaminones, oximes, and the isoxazole heterocycle. The cell growth inhibitory and apoptosis inducing effects of the new analogs were evaluated by in vitro assays in the hepatocellular carcinoma HA22T/VGH cells, as well as in the MCF-7 breast cancer cell line and in its multidrug resistant (MDR) variant MCF-7R. Increased antitumor activity on all cell lines was found with the isoxazole analog and especially with the benzyl oxime derivative; in the HA22T/VGH cell model, the latter compound inhibited constitutive NF-κB activation.

Cell growth inhibitionSpectrometry Mass Electrospray IonizationCurcuminMagnetic Resonance SpectroscopyMDR breast cancer cellsClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsBiochemistrychemistry.chemical_compoundCell Line TumorDrug DiscoveryNF-κB inhibitionHumansIsoxazoleCytotoxicityMolecular BiologyChromatography High Pressure LiquidCell growthOrganic ChemistryCell growth inhibition; Curcumin oxime derivatives; MDR breast cancer cells; NF-κB inhibition;KetonesCurcumin oxime derivativesDrug Resistance MultipleMultiple drug resistancechemistryBiochemistryDrug Resistance NeoplasmCell cultureApoptosisCancer cellSettore BIO/14 - FarmacologiaCurcuminMolecular MedicineCellBioorganic & Medicinal Chemistry Letters
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Cajanol, a novel anticancer agent from Pigeonpea [Cajanus cajan (L.) Millsp.] roots, induces apoptosis in human breast cancer cells through a ROS-med…

2010

Cajanol (5-hydroxy-3-(4-hydroxy-2-methoxyphenyl)-7-methoxychroman-4-one) is an isoflavanone from Pigeonpea [Cajanus cajan (L.) Millsp.] roots. As the most effective phytoalexin in pigeonpea, the cytotoxic activity of cajanol towards cancer cells has not been report as yet. In the present study, the anticancer activity of cajanol towards MCF-7 human breast cancer cells was investigated. In order to explore the underlying mechanism of cell growth inhibition of cajanol, cell cycle distribution, DNA fragmentation assay and morphological assessment of nuclear change, ROS generation, mitochondrial membrane potential (DeltaPsim) disruption, and expression of caspase-3 and caspase-9, Bax, Bcl-2, PA…

Cell growthCytochrome cApoptosisBreast NeoplasmsGeneral MedicineMitochondrionCell cycleBiologyToxicologyFlow CytometryMolecular biologyAntineoplastic Agents PhytogenicIsoflavonesPlant RootsMitochondriaCajanusCell cultureApoptosisCell Line TumorCancer cellbiology.proteinCytotoxic T cellHumansFemaleReactive Oxygen SpeciesChemico-biological interactions
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PON3 is upregulated in cancer tissues and protects against mitochondrial superoxide-mediated cell death

2012

To achieve malignancy, cancer cells convert numerous signaling pathways, with evasion from cell death being a characteristic hallmark. The cell death machinery represents an anti-cancer target demanding constant identification of tumor-specific signaling molecules. Control of mitochondrial radical formation, particularly superoxide interconnects cell death signals with appropriate mechanistic execution. Superoxide is potentially damaging, but also triggers mitochondrial cytochrome c release. While paraoxonase (PON) enzymes are known to protect against cardiovascular diseases, recent data revealed that PON2 attenuated mitochondrial radical formation and execution of cell death. Another famil…

Cell signalingProgrammed cell deathMAP Kinase Signaling SystemApoptosisMitochondrionBiologyEndoplasmic ReticulumGene Expression Regulation EnzymologicMicechemistry.chemical_compoundSuperoxidesNeoplasmsAnimalsHumansMolecular BiologyOriginal PaperAryldialkylphosphataseSuperoxideCytochromes cCell BiologyMitochondriaNeoplasm ProteinsUp-RegulationCell biologyGene Expression Regulation NeoplasticHEK293 CellschemistryApoptosisCancer cellDNAJA3Signal transductionCell Death & Differentiation
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p53 as the main traffic controller of the cell signaling network

2010

Among different pathological conditions that affect human beings, cancer has received a great deal of attention primarily because it leads to significant morbidity and mortality. This is essentially due to increasing world-wide incidence of this disease and the inability to discover the cause and molecular mechanisms by which normal human cells acquire the characteristics that define cancer cells. Since the discovery of p53 over a quarter of a century ago, it is now recognized that virtually all cell fate pathways of live cells and the decision to die are under the control of p53. Such extensive involvement indicates that p53 protein is acting as a major traffic controller in the cell signa…

Cell signalingSettore MED/06 - Oncologia MedicaApoptosisDiseaseCell fate determinationBiologyNeoplasmsmedicineApoptosis; Cellular Senescence; Gene Expression Regulation Neoplastic; Humans; Mutation; Neoplasms; Polymorphism Genetic; Signal Transduction; Tumor Suppressor Protein p53HumansCellular SenescencePolymorphism GeneticCancerApoptosiCell cyclemedicine.diseaseCell biologyGene Expression Regulation NeoplasticThe Hallmarks of CancerApoptosisCancer cellMutationNeoplasmTumor Suppressor Protein p53HumanSignal Transduction
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Synthesis and Antitumor Properties of 2,5-Bis(3'-indolyl) thiophenes: Analogues of Marine Alkaloid Nortopsentin

2007

A series of 11 bis-indolylthiophenes of formula I were obtained by cyclization of bis-indole 1,4-diketones using Lawesson''s reagent. Derivs. I (R = OMe, R1 = SO2Ph), I (R = OMe, R1 = Me), I (R = Cl, R1 = Me), and I (R = OMe, R1 = H) were selected to be evaluated in the full panel of about 60 human tumor cell lines derived from nine human cancer cell types and showed antiproliferative activity generally in the micromolar range. The most sensitive cell lines were: CCRF-CEM, MOLT-4, HL60 (TB), and RPMI-8226 of the leukemia subpanel, HT29 and HCC-2998 cell lines of the colon sub-panel, NCI-H522 of the non-small cell lung cancer sub-panel, LOX IMVI of the melanoma sub-panel, and UO-31 of the re…

Cell typeIndolescyclizationHL60StereochemistryClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsThiophenesBiochemistryChemical synthesisInhibitory Concentration 50chemistry.chemical_compoundAlkaloids5-bis(3'-indolyl)thiophenesCell Line TumorDrug DiscoverymedicineAnimalsHumansantitumor activityMolecular BiologyCell Proliferationbis-indolylthiopheneCell growthNortopsentinMelanomaOrganic ChemistryImidazolesCancerBiological activityDNAmedicine.diseasediketonesTopoisomerase II5-bis(3'-indolyl)thiophenes; antitumor activity; Topoisomerase II; NortopsentinDNA Topoisomerases Type IIchemistryCell cultureMolecular Medicine
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Powerful tumor cell growth-inhibiting activity of a synthetic derivative of atractyligenin: Involvement of PI3K/Akt pathway and thioredoxin system

2014

The semi-synthetic ent-kaurane 15-ketoatractyligenin methyl ester (SC2017) has been previously reported to possess high antiproliferative activity against several solid tumor-derived cell lines. Our study was aimed at investigating SC2017 tumor growth-inhibiting activity and the underlying mechanisms in Jurkat cells (T-cell leukemia) and xenograft tumor models. METHODS: Cell viability was evaluated by MTT assay. Cell cycle progression, reactive oxygen species (ROS) elevation and apoptotic hallmarks were monitored by flow cytometry. Inhibition of thioredoxin reductase (TrxR) by biochemical assays. Levels and/or activation status of signaling proteins were assessed by western blotting. Xenogr…

CellBiophysicsAntineoplastic AgentsApoptosisAtractylosideBiologyCell cycleBiochemistryJurkat cellsMicePhosphatidylinositol 3-KinasesThioredoxinsTumor Cells CulturedmedicineAnimalsHumansMTT assayViability assaySettore BIO/15 - Biologia FarmaceuticaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationPI3K/AktHCT 116 xenograftCytochromes cApoptosiThioredoxin systemSettore CHIM/06 - Chimica OrganicaCell cycleXenograft Model Antitumor AssaysCell biologymedicine.anatomical_structureCaspasesCancer researchThioredoxinDiterpenes KauraneProto-Oncogene Proteins c-aktEnt-kaurane
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PTHrP [67-86] regulates the expression of stress proteins in breast cancer cells inducing modifications in urokinase-plasminogen activator and MMP-1 …

2003

It was previously reported that a midregion domain of parathyroid hormone-related protein (PTHrP), that is, [67-86]-amide, is able to restrain growth and promote matrigel penetration by the 8701-BC cell line, derived from a biopsy fragment of a primary ductal infiltrating carcinoma of the human breast, and that cell invasion in vitro is drastically impaired by inactivation of urokinase-plasminogen activator (uPa). In this study we started a more detailed investigation of the possible effects on gene expression arising from the interaction between PTHrP [67-86]-amide and 8701-BC breast cancer cells by a combination of conventional-, differential display-and semi-quantitative multiplex-polyme…

CellBreast NeoplasmsBiologyHeat Shock Transcription FactorsDownregulation and upregulationCell Line TumorHeat shock proteinmedicineHumansNeoplasm InvasivenessHSP90 Heat-Shock ProteinsEnzyme InhibitorsHSF1Heat-Shock ProteinsMatrigelActivator (genetics)CarcinomaParathyroid Hormone-Related ProteinCell BiologyOligonucleotides AntisenseUrokinase-Type Plasminogen ActivatorMolecular biologyPeptide FragmentsProtein Structure TertiaryUp-RegulationDNA-Binding ProteinsGene Expression Regulation NeoplasticHeat shock factormedicine.anatomical_structureCell cultureCancer researchFemaleQuercetinMatrix Metalloproteinase 1Transcription FactorsJournal of Cell Science
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High expression of QSOX1 reduces tumorogenesis, and is associated with a better outcome for breast cancer patients.

2012

International audience; ABSTRACT: INTRODUCTION: The gene quiescin/sulfhydryl oxidase 1, QSOX1, encodes an enzyme directed to the secretory pathway and excreted into the extracellular space. QSOX1 participates in the folding and stability of proteins and thus could regulate the biological activity of its substrates in the secretory pathway and/or outside the cell. The involvement of QSOX1 in oncogenesis has been studied primarily in terms of its differential expression in systemic studies. QSOX1 is overexpressed in prostate cancers and in pancreatic adenocarcinoma. In contrast, QSOX1 gene expression is repressed in endothelial tumors. In the present study, we investigated the role of QSOX1 i…

CellGene ExpressionBreast Neoplasms[SDV.CAN]Life Sciences [q-bio]/CancerBiologymedicine.disease_causeMetastasis[ SDV.CAN ] Life Sciences [q-bio]/CancerMice03 medical and health sciences0302 clinical medicineBreast cancer[SDV.CAN] Life Sciences [q-bio]/CancerCell MovementCell Line TumormedicineExtracellularAnimalsHumansOxidoreductases Acting on Sulfur Group DonorsRNA MessengerNeoplasm MetastasisCell ProliferationRetrospective Studies030304 developmental biologyMedicine(all)0303 health sciencesCell growthCancermedicine.diseaseExtracellular MatrixTumor Burden3. Good healthPatient Outcome AssessmentDisease Models AnimalProtein TransportCell Transformation Neoplasticmedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchHeterograftsAdenocarcinomaFemaleNeoplasm GradingCarcinogenesisResearch Article
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Structural and regulatory functions of keratins.

2007

The diversity of epithelial functions is reflected by the expression of distinct keratin pairs that are responsible to protect epithelial cells against mechanical stress and to act as signaling platforms. The keratin cytoskeleton integrates these functions by forming a supracellular scaffold that connects at desmosomal cell-cell adhesions. Multiple human diseases and murine knockouts in which the integrity of this system is destroyed testify to its importance as a mechanical stabilizer in certain epithelia. Yet, surprisingly little is known about the precise mechanisms responsible for assembly and disease pathology. In addition to these structural aspects of keratin function, experimental e…

CellIntermediate Filamentsmacromolecular substancesBiologyFocal adhesionEpidermolysis bullosa simplexMicrotubuleOrganelleKeratinmedicineAnimalsHumansCytoskeletonCytoskeletonchemistry.chemical_classificationCell PolarityEpithelial CellsCell BiologyDesmosomesmedicine.diseaseCell biologymedicine.anatomical_structureCell Transformation NeoplasticchemistryKeratinsStress MechanicalFunction (biology)Signal TransductionExperimental cell research
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Estradiol decreases xanthine dehydrogenase enzyme activity and protein expression innon-tumorigenicand malignant human mammary epithelial cells

2009

The retinoic acid deficiency in breast tumour epithelial cells has been ascribed to an insufficient expression of either the enzyme(s) involved in its biosynthesis or the cellular retinol binding protein (CRBP) or both. In an attempt to define the mechanisms underpinning retinoic acid deficiency in these cell model systems, we have investigated the potential regulatory effect of oestrogen (17β-estradiol) on one key player in retinoic acid biosynthesis, the xanthine dehydrogenase (XDH). This enzyme is consistently expressed and very active in non-malignant human mammary epithelial cells (HMEC), as opposed to tumour MDA-MB231 and MCF7 cells. In these latter two cell lines, as opposed to HMEC …

CellRetinoic acidTretinoinBiologyBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaRETINOIC ACIDmedicineHumansRNA MessengerMammary Glands Humanskin and connective tissue diseasesXanthine oxidaseXANTHINE OXIDASEESTRADIOLMolecular BiologyRetinolEpithelial CellsCell BiologyMolecular biologyEnzyme assayGene Expression Regulation NeoplasticRetinoic acid receptormedicine.anatomical_structurechemistryXanthine dehydrogenaseCell culturebiology.proteinXANTHINE DEHYDROGENASEJournal of Cellular Biochemistry
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